The genesis of the instant invention was in the multiple deficiencies that the Applicants found with existing intra-cochlear hearing aid implants of the ear. To understand the issues that give rise to the need for implantable hearing aids, it is helpful to first understand the anatomy and physiology of the ear, and in particular, the cochlea and its associated structures.
Referring to FIG. 3, there is shown a sectional view of the anatomy of the human auditory system A. At a macro level, the human auditory system A consists of the outer ear 0, the middle ear M, and the inner ear I. The outer ear 0 includes the pinna or auricle 21 and the ear canal 25 that provides communication from the outer ear 0 to the middle ear M. The middle ear M includes the eardrum (tympanic membrane) 10, the ossicles 17 consisting of the hammer (malleus bone) 24, the anvil (incus bone) 19, and the stirrup (stapes bone) 20, with the stapes tendon 11 providing support for the ossicles 17, and the eustachian tube 26. The middle ear M also includes the oval window 12 to which is attached the stirrup 20 for communication there through and the round window 18 which provides communication with the scala tympani ST.
The inner ear has two main components which are the semi-circular canals 22 and the cochlea 30. The endosteum 9 lines the entire inner surface of the inner ear I. The cochlea 30 includes the scala tympani ST, the scala media SM and the scala vestibuli SV. The perilymphatic chamber of the vestibular system has a wide connection to scala vestibuli SV, which in turn connects to scala tympani 14 by an opening called the helicotrema 16 at the apex of the cochlea 30. The scala tympani ST is then connected to the cerebrospinal fluid of the subarachnoid space by the cochlear aqueduct. The cochlear nerve AN sometimes referred to as Auditory Nerve AN extends from the cochlea 30 to the brain.
The reader's attention is directed to FIGS. 1 and 1A, which illustrate the cochlea. As a background, the Organ of Corti is denoted by “OC” in FIGS. 1 and 1A. (FIGS. 1 and 1A were taken from www.hoorzaken.nl/de_cochlea.htm and www.wikipedia.org.).
The cochlea is a spiraled, hollow conical chamber of bone. Its structures include the scala vestibuli SV which contains perilymph and lies superior to the cochlear duct and abuts the oval window. The scala tympani ST contains perilymph, and lies inferior to the scala media and terminates at the round window. The scala media SM contains endolymph, and is the membraneous cochlear duct containing the Organ of Corti OC. The helicotrema is the location where scala tympani ST and the scala vestibuli SV merge. The Reissner's membrane RM separates the scala vestibuli SV from the scala media SM. The basilar membrane BM separates the scala media SM from the scala tympani ST.
The Organ of Corti OC is the peripheral end-point of the hearing nerves and contains hair cells and other cellular anatomy. The Organ of Corti is where the mechanical energy of sound waves is transformed into the electrical energy of nerve impulses. The Organ of Corti transforms mechanical sound energy into electrical stimuli which the ganglion cells carry to the cochlear nerve (also known as the Auditory Nerve AN) and then to the brain. In a deaf person, the Organ of Corti is either non-functional or is missing. In many deafness pathologies, the cochlear duct, which is the fluid space that contains the Organ of Corti, becomes devoid of functioning anatomy, and it is basically a non-functional fluid space. Even though the ear bones are vibrating and the inner ear fluids are vibrating, if the Organ of Corti is not functioning, then mechanical energy cannot be turned into electrical energy.
In some respects, the Organ of Corti operates much like a microphone head in that it picks up the sound wave energy and converts it to electrical energy. The nerves from the Organ of Corti travel along the osseous spiral lamina back to the spiral ganglion and from there, they continue by way of the cochlear nerve into the brain. In a hearing impaired person, the anatomy within the cochlear duct is often destroyed. In other words, the Organ of Corti does not function since there are no anatomical parts to perform any functions. It is analogous to having the head of the microphone cut off or destroyed.
When the Organ of Corti is functionally dead, nerves degenerate along the osseous spiral lamina and back to the spiral ganglion. One can look at the spiral ganglion as the wire that feeds the microphone and which terminates at the microphone head or Organ of Corti. Aiding the non-functional ear by using a hearing device known as a cochlear implant substitutes an electronic device for the Organ of Corti. The electrical device directly electrically stimulates the remaining nerve elements with an electrical pulse analogous to the function of the Organ of Corti. Because one no longer has the microphone head-like Organ of Corti to transduce mechanical sound energy to an electrical signal energy. What one is doing by employing a cochlear implant is delivering electrical impulses directly into the “wire of the microphone” or in this case, the spiral ganglion.
If any of these structures are damaged, normal function of the overall hearing mechanism is decreased. Further, when medical care of hearing loss is rendered, specifically with cochlear implantation, if the anatomic structures, in addition to the Organ of Corti, are decreased in number or not present to transmit the stimulus provided by the implant, a poor result would be expected from the cochlear implant. Thus, maximal presence of the internal anatomy of the cochlea and its related structures is paramount in restoring hearing through the use of a cochlear implant.
Prior art intra-cochlear implants exist, and were first seen in the late 1950s and early 1960s. A typical prior art intra-cochlear implant 99 is shown schematically in FIG. 2. Other examples of prior art intra-cochlear implants are shown in the patents cited in the application file. When cochlear implants were first being conceived and tested, it was not known how best to approach the cochlear nerve with the electrical impulse electrode studs. Some people felt that it was preferable to provide an intra-cochlear implant that was placed within the scala tympani or scala vestibuli, whereas others believed it preferable to employ an extra-cochlear implant that was placed exteriorly of the scala tympani and scala vestibuli. The extra-cochlear electrodes, which are not the subject at hand, at that time were basically placed on the unaltered or minimally altered bone of the cochlea and then secured to the bone. An improved extra-cochlear implant is shown in Fritsch et al., co-pending U.S. patent application Ser. No. 11/451,715 filed 13 Jun. 2006.
Intra-cochlear implants, of the types that this patent application addresses have to transmit electrical signals through the cochlear fluids of the scala vestibuli or scala tympani and the bone of the modiolus to reach the residual dendrites and spiral ganglia nerve cells.
One of the problems in dealing with intra-cochlear implants is that the small size of the inner ear structures such as the Organ of Corti, dendrites, spiral ganglion cells, and all the other anatomic structures within the cochlea severely limits the size of any intra-cochlea implant.
Returning to FIGS. 1,1A and 2, the usual intra-cochlear implant is preferably placed within the scala tympani ST of the cochlea although it can also be placed in the scala vestibuli SV. However, as the implant is relatively large and stiff, as it coils through the cochlea, the implant can act like a bulldozer that may penetrate through, rip and even strip out the other membranes and the lining endosteum, including everything from dendrites, osseous spiral lamina, vestibular ligament, spiral ligament, basilar membrane BM, stria vasularis, and to the Corti's organ OC of hearing. Such implant-induced damage deleteriously impacts the performance of the spiral ganglion SG and the cochlear nerve AN that are in the modiolus. The spiral ganglion SG is an important structure because this is where residual nerve cells in sensory hearing loss reside and are those that initiate transmission of the implant's electrical impulse to the cochlear nerve AN and eventually to the brain. Thus, an intra-cochlear implantation technique can be very traumatic and reduce the ability of the implant to successfully stimulate residual neural elements in patients with hearing loss. FIG. 2 diagrammatically shows the prior art implant electrode wire 100 of an intra-cochlear implant attached to the electrode 102 with stimulating points 103 within the cochlea.
Over time, technology has progressed, and improvements have been made in intra-cochlear implants. Currently, there exist three major manufacturers of intra-cochlear implanted hearing aid devices, including Cochlear Corporation (Melbourne, Australia); Med-El Corporation (Innsbruck, Austria); and Advance Bionics, which is now a unit of Boston Scientific Co. (Natick, Mass., USA).
Some implants now manufactured are slimmer, more flexible and designed to help overcome the initial problems of stiffness which caused great degrees of trauma. There may be lesser degrees of trauma with these newer implants although the damage they can potentially cause is still considerable. A typical implant will go into the cochlea up to about 20-30 mm, although some of them only go in up to 6 mm. The cochlea measures about 36 mm. in length. FIGS. 2 and 3 show a basic schematic of an intra-cochlear implant position and some ear macro-anatomy. It should be noted that with increasing loss of function and degeneration of the Organ of Corti, there is a serial degeneration seen in the dendrites and spiral ganglion cells. Thus, even without cochlear implant insertion trauma, suboptimal numbers of dendrites and spiral ganglion cells will be present. Indeed, there is a direct correlation between hearing loss within the audiometric spectrum and loss of anatomic structure. Implant insertion trauma further adds to the degeneration and loss of neural elements such as the dentrites and spiral ganglion cells.
Another major problem with present implants is that they have a relatively limited number of electrodes from which to stimulate the cochlea. Intra-cochlear implants known currently to Applicants range from one to 24 mono or bipolar electrodes. The number of original cells within the human Organs of Corti that stimulate the spiral ganglion cells and cochlear nerve are in the tens of thousands (˜30,000). Thus, a major deficiency of present implants is that they do not adequately stimulate in numbers all along the cochlea. The result is lack of resolution within the sound-perception spectrum. Each single electrode substitutes for thousands of originally functioning cells.
Another major problem with presently available implants is that they do nothing to help regenerate any of the anatomic deficiencies just described. With present implants there are no means of delivering chemicals, medications, nutrients, nucleotides, and cells into the cochlea and/or perfusion of these substances and cells into and out of the cochlea.
Another deficiency with presently available implants is that electrical stimulus transmission is not transmitted from an electrode stud to a nerve structure by directly touching or even being intimate to one. Presently manufactured implants have intra-cochlear electrodes that must traverse fluid and bone to reach residual nerve tissue elements. Compared to directly touching nerve elements, it takes an extraordinary amount of electrical stimulation energy to appropriately stimulate the spiral ganglia and nerve cells through fluid and bone. Also, there is dispersion of the electrical energy from the electrode stud that causes the electrical signals to impact a wide area, and hence a large number of ganglia, as opposed to a small specific point on the cochlea. Additionally, the farther away the electrode studs are from the nerve elements, the more electrical power is required and used.
The cochlea is organized “tonotopically”. In other words, specific tone frequencies are found at specific points along the length of the cochlea. At the cochlear basal turn, the cochlear duct membranes and their adjacent ganglion and nerve cells are where those ganglia and receptors are positioned that are designed for being receptive to high frequencies and at the very apex, the cochlear duct areas are where those ganglia are positioned that are receptive to the lowest frequencies are located. Thus, when one inserts a cochlear implant close to the round window in the usual cochleostomy procedure, the implant first will advance past the cochlear parts that stimulate high frequencies, then advance through the mid-frequencies and then to the lower frequencies.
Because of the tonotopic anatomy, if one puts a broadly dispersed electrical stimulus impulse into the cochlea, the impulse will impact spiral ganglion cells that cover a wide tonotopic range, and will not be as tonally specific. Rather than sampling a very narrow frequency spectrum of the tonotopic arrangement the impulse would then stimulate a very wide swath of frequencies.
Therefore, a major deficiency of the intra-cochlear implant prior art is the relatively low number of stimulating electrode points that are placeable on an implant. If one has a greater number of electrode studs, then one has more electrode spots on the implant with which to stimulate more individual nerve elements. Increasing the number of stimulated spots in the cochlea has the potential to result in more frequency differentiation and sound understanding which would likely result in a more accurate auditory experience for the user. Also, the more closely the stimulating electrode studs are positioned to the residual ganglion nerve cells, the more likely that the electrical signal output of the studs are to be focused on the ganglion cells of interest for that particular tone. Conversely, the greater the distance between stud and targeted ganglia, the more likely the stimuli will get dispersed and not impact the ganglion cells of interest, but rather impact ganglion cells over a wide tonal section.
The internal cochlear implants that exist now serve their intended function to a limited extent. However, room for improvement exists to provide an intra-cochlear implant that overcomes one or more of the preliminary deficiencies of current, known implants. As alluded to above, the primary drawbacks of current known implants are: (1) the internal destruction they cause to the cochlea; (2) the size limitations that they impose; (3) the lack of tonal and tonotopic specificity; (4) the lack of direct nerve touching electrical stimulation; and (5) the lack of a mechanism to achieve anatomic regeneration. One of the vexing problems that face those designing implants is the limitations that exist on the potential size of implant. Implant size limitations exist because there is only so much internal diameter to the cochlea to allow an electrode to pass. Thus, current technology only allows for so many electrode stimulating studs inside the cochlea because the sum diameter of the many numbers of wires to the electrode studs is limited by the cochlear diameter. The electrode sizes are destructively large and stiff. Additionally, the space limitations do not allow for perfusion hardware and cell-nerve regeneration techniques within the cochlea.
One object of the present invention is to provide an intra-cochlear implant that overcomes or at least reduces the severity of one or more of the deficiencies described above, of prior art intra-cochlear implants.